Effect of tumor necrosis factor-alpha on experimental otitis media with effusion

Abstract

Objectives/hypothesis: Up to the present, many reports have demonstrated that local immune response is associated with maintenance and persistence of effusion in the middle ear cavity. Resulting retention of inflammatory cells and mediators in the middle ear results in ongoing effusion. The purpose of this study was to clarify the role of tumor necrosis factor in experimental otitis media with effusion, which was induced by transtympanic injection of tumor necrosis factor in the rats.

Study design: Four groups were designed in two experiments. The purpose of experiment 1 was to confirm that transtympanic injection of TNF-alpha produces the middle ear effusion. In experiment 2, TNFsolRI was used to evaluate the possibility as an inhibitor in otitis media with effusion.

Methods: The histopathological changes were observed under light microscope, and the changes in microvascular permeability were examined using Evans blue vital dye technique.

Results: Middle ear effusion was developed in 70% of specimens, and histopathological changes, such as subepithelial edema and marked infiltration of neutrophils, were present in 100% at 24 hours after administration of tumor necrosis factor-alpha through transtympanic approach. Extravasation of Evans blue dye was found in all specimens injected by tumor necrosis factor-alpha, which was qualified using a fluorescence microscope and quantified using a spectrophotometer. These histopathological findings and changes in microvascular permeability were significantly reduced by tumor necrosis factor soluble receptor type I.

Conclusions: Neutrophil infiltration, subepithelial edema, increased microvascular permeability, and resultant effusion were indirectly proved to be induced by tumor necrosis factor-alpha. We hope that this study may contribute to understanding the role of tumor necrosis factor-alpha in otitis media with effusion and clarifying the future role of tumor necrosis factor soluble receptor type I in preventing otitis media with effusion.